ArticleNpj biological timing and sleep2026
Modelling the effect of V1a receptor antagonism and its potential therapeutic effect in circadian disorders.
Article in Npj biological timing and sleep, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The suprachiasmatic nucleus (SCN) is the central circadian clock in mammals, and its dysregulation is linked to various circadian disorders. Vasopressin signaling is a primary regulator of SCN synchronicity and functional output. We investigated the effect of the V1a receptor (V1aR) antagonist, balovaptan (30 mg/kg), on locomotor activity rhythms in mice following a 6-hour phase advance of the light-dark cycle. We found that a single administration significantly accelerated resynchronization of locomotor rhythms. To investigate the underlying mechanism, we developed a mathematical framework simulating the SCN and its control of biomarkers, including melatonin and core body temperature. Our model successfully captures the accelerated synchronization observed under V1aR antagonism and replicates well-established SCN behaviors, such as the phase response curve and forced desynchronization. Mechanistically, the model suggests that weakening vasopressin signaling strengthens the SCN's resistance to internal desynchronization. Furthermore, we show a strong link between the endogenous period and the phase of circadian biomarkers. The model predicts that V1aR antagonism induces a phase advance proportional to the endogenous period, suggesting that individuals with longer endogenous periods may experience more substantial therapeutic benefits. This framework establishes a computational foundation for designing clinical trials evaluating V1aR antagonism for circadian rhythm disorders.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.